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Regulation of CD4+ T Cells by Pleural Mesothelial Cells via Adhesion Molecule-Dependent Mechanisms in Tuberculous Pleurisy.
- Source :
- PLoS ONE; Sep2013, Vol. 8 Issue 9, p1-1, 1p
- Publication Year :
- 2013
-
Abstract
- Background:Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been demonstrated to be expressed on pleural mesothelial cells (PMCs), and to mediate leukocyte adhesion and migration; however, little is known about whether adhesion molecule-dependent mechanisms are involved in the regulation of CD4<superscript>+</superscript> T cells by PMCs in tuberculous pleural effusion (TPE). Methods:Expressions of ICAM-1 and VCAM-1 on PMCs, as well as expressions of CD11a and CD29, the counter-receptors for ICAM-1 and VCAM-1, respectively, expressed on CD4<superscript>+</superscript> T cells in TPE were determined using flow cytometry. The immune regulations on adhesion, proliferation, activation, selective expansion of CD4<superscript>+</superscript> helper T cell subgroups exerted by PMCs via adhesion molecule-dependent mechanisms were explored. Results:Percentages of ICAM-1-positive and VCAM-1‒positive PMCs in TPE were increased compared with PMC line. Interferon-γ enhanced fluorescence intensity of ICAM-1, while IL-4 promoted VCAM-1 expression on PMCs. Percentages of CD11a<superscript>high</superscript>CD4<superscript>+</superscript> and CD29<superscript>high</superscript>CD4<superscript>+</superscript> T cells in TPE significantly increased as compared with peripheral blood. Prestimulation of PMCs with anti‒ICAM-1 or ‒VCAM-1 mAb significantly inhibited adhesion, activation, as well as effector regulatory T cell expansion induced by PMCs. Conclusions:Our current data showed that adhesion molecule pathways on PMCs regulated adhesion and activation of CD4<superscript>+</superscript> T cells, and selectively promoted the expansion of effector regulatory T cells. [ABSTRACT FROM AUTHOR]
- Subjects :
- TUBERCULOSIS patients
CD4 antigen
T cells
MESOTHELIUM
CELL adhesion
INTERFERONS
Subjects
Details
- Language :
- English
- ISSN :
- 19326203
- Volume :
- 8
- Issue :
- 9
- Database :
- Complementary Index
- Journal :
- PLoS ONE
- Publication Type :
- Academic Journal
- Accession number :
- 90531986
- Full Text :
- https://doi.org/10.1371/journal.pone.0074624